Interleukin–13 ameliorates postischemic hepatic gluconeogenesis and hyperglycemia in rat model of stroke
by Ronald
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Hyperglycemia is a well-known indicator of stroke prognosis, and a third of non-diabetic patients develop hyperglycemia postischemic during the acute phase of stroke; This relates to the relatively poor prognosis, high mortality, and impaired neurological recovery. Interleukin-13 (IL-13), a member of the family of Th2 cytokines, which are involved in the regulation of immune responses and metabolism of glucose.
Thus, we investigated the mechanism of postischemic hyperglycemia and the role of IL-13 by using a rat model of permanent middle cerebral artery occlusion (MCAO). Our results show that hyperglycemia and hyperinsulinemia postischemic accompanied by an increase in HOMA-IR, elevated hepatic gluconeogenesis and reduced insulin signaling.
A shift in the direction of the inflammatory response was evident with the results of the elevated proinflammatory cytokines and increased expression of negative regulatory proteins, indicating an ongoing vicious cycle of insulin-resistant hyperglycemia induced inflammation. IL-13 treatment counteracted proinflammatory state and eliminate a vicious circle through increased stat-6 and STAT3, which mediated immune and metabolic pathways respectively;
This effect resolved pathological changes previously described postischemic hyperglycemia and reduced infarct size in rat MCAO. Our findings show the importance of Th1-Th2 balance in peripheral glucose metabolism affected by acute ischemic stroke, which gives a new perspective to the prevention and control of hyperglycemia postischemic.
Interleukin–13 ameliorates postischemic hepatic gluconeogenesis and hyperglycemia in rat model of stroke
interleukin – 13 receptor subunit alpha-2 is the target of the progesterone receptor and koaktivator steroid receptor-1 in rat uterus
Endometrium, composed of epithelial and stromal cell compartment, closely regulated by ovarian steroid hormones estrogen (E2) and progesterone (P4) during early pregnancy. Through the progesterone receptor (PGR), steroid receptor coactivators, and other transcription coregulators, progesterone inhibits the E2-induced cell proliferation and induce differentiation of stroma cells in a process called decidualizing to promote the acceptance of the endometrium.
Although the interleukin-13 receptor subunit alpha-2 (Il13ra2) is expressed in human and mouse endometrium, the potential role of steroid hormones in the regulation of endometrial not yet been thoroughly researched. In this study, we employ PGR KO mice (PRKO) and koaktivator steroid receptor-1 knockout mice (SRC-1 – / -) to Il13ra2 expression profile in murine endometrium and decisive role in the transcriptional regulator of hormone responsive Il13ra2 expression. In addition, we utilized decidualizing-inducing cocktail steroidogenic established and based siRNA knockdown of IL13RA2 to determine the importance decidualizing IL13RA2 in primary human endometrial stromal cells.
Our findings indicate that Il13ra2 stated in sub-epithelial endometrial stromal murine ovarian steroid hormones in response to and during early pregnancy by PGR- and SRC-1-dependent. In addition, we demonstrated that knockdown of IL13RA2 before in vitro human endometrial stromal cells decidualizing main portion decidualizing compromise full response. We conclude that Il13ra2 is a downstream target of progesterone through PGR and SRC-1 and plays a role in mediating the action of stromal ovarian steroid hormones.
Lung function did not significantly differ between the three groups before treatment. After treatment, the time to relief of symptoms was significantly shorter in the GG group than that in the other two groups. forced expiratory volume in one second expiratory flow and percent predicted peak was also significantly better in the GG group compared to the other two groups.
